Field of the Invention
The present invention relates generally to visual recognition in human subjects, and, more particularly, to promoting automatic recognition of sight words via generation of non-verbal stimuli that manipulate dyslexics' and poor readers' visual spatial attention.
Background Art
At a first glance, reading seems almost magical: our gaze lands on orthographic signs lying in serial order next to each other, and our brains effortlessly give us access to their meaning and pronunciation. However, reading is far from simple. It is an exceptionally complicated task that involves visual processing and optomotor functions. In order to read, our brain recruits in just about 280 milliseconds, neural networks scattered in many different and distant regions of the cortex across both brain hemispheres.
Reading starts in the central part of the retina, called the fovea, an area dense in high-resolution photoreceptor cells which are sensitive to light. The fovea occupies about 13 degrees of the visual field, and is the only part of the retina that is truly useful for reading. The need for printed text to reach the fovea explains why reading is a dynamic motion task. Our eyes don't sweep a text in a constant fashion, quite the contrary; they sweep a text in small steps/leaps called saccades. Our eyes attain a quasi-stationary state called a fixation that lasts about 220-300 milliseconds for familiar words or up to 500 milliseconds for unfamiliar words. When the eyes fixate, visual information can be extracted and decoded for meaning. During a fixation, the eyes have access to three regions: the foveal, the parafoveal, and the peripheral. The foveal region is the area with the sharpest acuity and includes 2 degrees of visual angle around the point of fixation, where 1 degree is equal to two or three letters (thus, four to six letters are in focus). The parafoveal region extends to about 15-20 letters, and the peripheral region includes everything in the visual field beyond the parafoveal region.
Visual precision is optimal at the center of gaze and gradually decreases towards the periphery since fewer cells are allocated to that portion of the visual scenery. In fact, our perceptual span enables us to identify only about ten or twelve letters per saccade: three or four to the left of the fixation point, and seven or eight to the right of the fixation point. Proficient readers make regressions to text already scanned about 10-15 percent of the time. The main difference between fast and slow readers is that the latter consistently show longer average fixation durations (350-500 milliseconds), shorter saccades, and more frequent regressions. In general, problems in oculomotor control have been considered in poor readers and dyslexics because they show an abnormal pattern of their fixation-saccadic eye movements during reading.
Mainstream scientific research theorizes that many of the reading anomalies observed in developmental dyslexia and in poor readers have been causally linked principally to the Posterior Parietal Cortex (PPC) and magnocellular deficit, but also, to a mild degree, to cerebellar deficits. Indeed, PPC seems to be the ‘crossroads of the brain’. See, Critchley M “The Parietal Lobes”, London, Hafner Press, (1953). It is generally accepted that the PPC is responsible for (a) sensorimotor integration. See, Goodale M A, Milner A D, “Sight unseen: An exploration of conscious and unconscious vision”. Oxford University Press, Oxford-New York, (2004); Milner A D, Goodale M A, “The Visual Brain in Action”, Oxford University Press, Oxford, (1995); Pisella L, Grea H, Tilikete C, Vighetto A, Desmurget M, Rode G, Boisson D, Rossetti Y, “An ‘Automatic Pilot’ for the hand in human posterior parietal cortex: Toward reinterpreting optic ataxia”, Nat. Neurosci 3: 729-736, (2000); (b) spatial attention. See, Bisley J W & Goldberg M E “Neuronal activity in the lateral intraparietal area and spatial attention”, Science 299:81-86, (2003a); Corbetta M & Shulman G L “Control of goal-directed and stimulus-driven attention in the brain,” Nat Rev Neurosci 3:201-215, (2002); Laberge D, “Attentional Control: Brief and prolong”. Psychol Res 66:230-233, (2002); Stein J, Glickstein M, “Role of the cerebellum in visual guidance of movement”. Physiol Rev 72:972-10.17, (1992); and (c) eye movement. See, Andersen R A “Visual and eye movement functions of the posterior parietal cortexa”. Ann Rev Neurosci 12:377-403, (1989); Bisley J W, Golberg M E, “The role of the parietal cortex in the neural processing of saccadic eye movements,” Adv Neurol 93: 141-157, (2003b). Dyslexics perform worse in tasks which are thought to be mediated by the PPC. For example, dyslexics have problems with spatial attention focusing (orienting), smooth pursuit of targets, temporal planning of fixations (stable gaze) and saccadic eye movements (e.g. saccadic inhibition) and demonstrate symptoms similar to those suffering from unilateral neglect (e.g. LHF inattention vs. RHF enhance recognition).
Eye movements and attention are closely related. The shift of attention from one object to another is usually followed by a saccade, i.e., a fast jump of the gaze aiming to foveate the new object of interest. Both an attention shift and the subsequent saccade are parts of the orienting response. To illustrate the latter, Biscaldi et al. measured saccadic eye movements in a single target (re-fixation) and in a sequential-target task (target jumped from one position to another). See, Biscaldi M, Gezeck S, Stuhr V, “Poor saccadic control correlates with dyslexia,” Neuropsychologia, 36:1189-1202, (1998). Their research indicated that, in relation to normal readers, dyslexics have much more scattered saccadic reaction times, i.e., many express saccades (i.e., saccades with latencies<135 misc.) and late saccades. They suggested that dyslexics' attentional shortcomings are responsible for their poorer saccadic control. In particular, they claimed that deficits in selective attention might result in deficits in fixation disengagements, and consequently in increased generation of late saccade and irregular saccade triggering.
The involvement of visual spatial attention in reading disorders has been clearly pointed out by Stein and Walsh. (See, Stein J, Walsh V, “To see but not to read; the magnocellular theory of dyslexia,” Trends Neurosci 20:147-152, 1997). Visual spatial attention research in developmental dyslexia suggests that mastery of reading fluency may be delayed or impaired due to lack of automatic and effortless sight words' identification. The lack of automatic and effortless sight words' identification is manifested in anticipation of letters, frequent errors in reading word endings, misplacement of letters within a word, hesitated, interrupted and slow reading. Accordingly, Facoetti et al suggested that visual disorders, often associated with dyslexia, might be determined by a deficit of spatial attention, that is, a deficit of the mechanisms that inhibit lateral information distraction (attentional focus deficit). See, Facoetti A, Paganoni P, Lorusso M L, “The spatial distribution of visual attention in developmental dyslexia,” Exp Brain Res 132:531-538, (2000a).
Still, additional studies centering on visual search tasks, have found that dyslexic children show poorer visual search performances in the left visual field (LVF) than in the right visual field (RVF), thus confirming asymmetric performances in dyslexic subjects. See, Eden G F, Stein J F, Wood F B, “Visuospatial ability and language processing in reading disabled and normal children,” In: Wright S F, Groner R (ed) “Studies in visual information processing: facets of dyslexia and its remediation”. North-Holland, Amsterdam, pp 321-335, (1993); Fowler M S, Richardson A J, Stein J F “Orthoptic investigation of neurological patients undergoing rehabilitation,” Br Orthoptic J 48:2-27 (1991). Hari and Koivikko suggested that compared with the RVF, dyslexics suffer from “mini-neglect” in the LVF. See, Hari R, Koivikko H, “Left-side mini-neglect and attentional sluggishness in dyslexic adult,” Soc Neurosci Abstr 25:1634, (1999). Based on Temporal Order Judgment (TOJ) research, showing a left-right asymmetry, Hari et al again hypothesized that dyslexics showed a LVF mini-neglect syndrome, a disadvantage of the left visual hemifield in selecting and processing visual information. See, Hari R, Renvall H, Tanskanen T “Left mini-neglect in dyslexic adults,” Brain 124: 1373-1380, (2001). According to Hari et al, the mini-neglect syndrome is caused by magnocellular deficit. See, Hari R, Renvall H, Tanskanen T “Left minineglect in dyslexic adults,” Brain 124: 1373-1380, (2001). Indeed, since the magnocellular system projects mostly to the parietal cortex, and the circuits controlling attention are located in the dorsal system, a diffuse functional disruption of the magnocellular pathway could weaken the input to this cortex. Moreover, the unilateral neglect syndrome usually stems from an impairment of the right, rather than the left, parietal cortex. Therefore, it seems reasonable to assume that generally weakened magnocellular input should result in a LVF disadvantage. This lateral spatial attention deficit in the LVF appears to be linked to a contralateral RVF enhancement in the processing of visual information, as demonstrated by an increased ability of dyslexics in letter recognition in the RVF. See, Geiger G, Lettvin J Y, Fahle M, “Dyslexic children learn a new strategy for reading: a controlled experiment,” Vision Res 34:1223-1233 (1994). A strong inhibition in the LVF (“mini-neglect” in the left visual field) could also hamper rapid and exact planning of regression saccades (backward movements from right to left) that is fundamental for fluent and correct reading and which is known to be altered in children with dyslexia. See, Morris R K, Rayner K “Eye movements in skilled reading: implications for developmental dyslexia”. In: Stein J F (ed) “Vision and visual dyslexia” MacMillan Press, London, 233-242 (1991).
Facoetti and Molteni also investigated the gradient of visual spatial attention in dyslexic children and in children with normal reading skills. Normally-reading children showed a normal symmetric distribution of spatial attention. In contrast, children with dyslexia showed an anomalous and asymmetric distribution of spatial attention. They hypothesized that a selective disorder of spatial attention is to blame for the spatial attention asymmetry (left inattention and right over-distractibility). See, Facoetti A, Molteni M, “The gradient of visual attention in developmental dyslexia,” Neuropsychologia 39:352-357 (2001). Indeed, dyslexics exhibited a reduced interference effect in the LVF (mild left inattention), associated with a strong interference effect in the RVF (right over-distractibility) See, Facoetti A, Turatto M, “Asymmetrical visual fields distribution of attention in dyslexic children: a neuropsychological study,” Neurosci Lett 290:216-218 (2000). An excessive inhibition of LVF stimuli (left inattention), associated with a lack of inhibition of RVF stimuli (right over-distractibility) may influence the automation skill necessary for effortless visuo-perceptual identification and decoding process of words, either by an anomalous suppression of identification of letters in the left side of a string, or by a difficulty in the inhibition of orienting visual attention (saccades) towards distracting visual peripheral stimuli coming from the RVF, which corresponds to the direction of reading of most languages.
Other evidence suggests that the magnocellular system, which plays a crucial role in the shifting of attention, is defective. See, Steinman B A, Steinman S B, Lehmkuhle S, “Transient visual attention is dominated by the magnocellular stream,” Vision Res 36:589-599 (1996); Stein J, Walsh V, “To see but not to read; the magnocellular theory of dyslexia,” Trends Neurosci 20:147-152 (1997). The Magnocellular system, which processes information about location and movement of visual stimuli, may affect reading by hampering the focus of attention (which requires precise coding of stimulus location). It has been shown that Magno cells dominate the dorsal-system projection from the primary visual cortex and further on to the parietal lobe's attentional and eye movement control regions. See, Livingstone M S, Hubei D H, “Segregation of form, color movement, and depth: anatomy, physiology and perception,” Science 240:740-749 (1988). Therefore, an impaired dorsal-system flow of visual information reaching the Posterior Parietal Cortex (PPC) is suspected of compromising visual attention orienting in dyslexic children. See, Vidyasagar T R, “A neural model of attentional spotlight: parietal guiding the temporal,” Brain Res Rev 30:66-76 (1999). Of relevance, Eden et al. found poor smooth pursuit, (smoothly tracking a slowly moving object in the visual field) in a dyslexic group, particularly when pursuing a target moving from left to right. Eden et al. proposed that eye-movement abnormalities might be due to the insufficient inhibition of Parvocellular activity from magnocellular activity. It should be also noted that left-right asymmetry reported by Eden et al. fits very well with the mini-neglect hypothesis. See, Eden G F, Stein J F, Wood M H, Wood F B, “Differences in eye movements and reading problems in dyslexic and normal children,” Vision Res 34:1345-1358 (1994).
Still on the magnocellular system involvement in eye movements and visual spatial attention, there is also a direct contribution of dorsal transient circuits to visuo-motor activity, or as Goodale et al. put it, there are two different kinds of vision: vision-for-perception and vision-for-action. Vision-for-action is thought to extract the information which is necessary for immediate use from the dorsal visual stream in fast motor actions and to rely on computations made mainly in the dorsal system. See, Goodale M A, Westwood D A, Milner A D, “Two distinct modes of control for object-directed action,” Prog Brain Res 144: 131-144 (2004).
Still on establishing a causal link between dyslexia and a deficit in the magnocellular system, there is strong research evidence suggesting that about two-thirds of dyslexic people have a low level deficit of the magnocellular visual system (Lovegrove, W., Martin, F., and Slaghuis, W. Atheoretical and experimental case for a visual deficit in specific reading disability, Cognitive Neuropsychol, 3, 225-67, 1986). Several studies have been conducted to compare the average performance of dyslexics to that of good readers. In general, these studies have found that: a) there is a reduced ability to detect flicker in dyslexic children, b) although there is a reduced ability to detect coarse detail, a normal ability was found to detect fine detail, c) there tends to be a prolonged persistence of the visual image, and d) dyslexic people have a decreased ability to detect fine motion. Additional studies discuss the higher perceptual outcomes level of magnocellular pathway impairment in dyslexic populations including perceptual grouping (Williams, M. C. and Bologna, N. B., Perceptual grouping in good and poor readers. Perception and Psychophysics 38, 367-375, 1985), (Solman, R. T., Cho, H., and Dain, S. J. Colour-mediated grouping effects in good and disabled readers, Ophtal. Physiol. Opt. 11, 320-7, 1991), sluggish foveal temporal processing, lack of inhibitory processes in peripheral visual processing spatial localization discrepancies Solman, R. T., May, J. G. Spatial localization discrepancies: a visual deficiency in poor readers, Am. J. Psychol. 103, 243-263, 1990), impaired visual temporal order judgment (May, J. G., Williams, M. C., Dunlap, W. P. Temporal order judgment in good and poor readers, Neuropsychologia 26, 917-24, 1988), improved visual search with target blurring, (Williams, M. C., May, J. G., Solman, R., Zhou, H. The effects of spatial filtering and contrast reduction on visual search times in good and poor readers, Vision Res., 35, 285-91, 1995) and impaired visual search when distractors are present (Visyasagar, T., R. Pammer, K. Impaired visual search in dyslexia relates to the role of the magnocellular pathway in attention, NeuroReport, 10, 1283-7, 1999).
Accordingly, what is desired are systems and methods that promote eye-hand coordination.